The mechanisms by which estrogens, ergot alkaloids and thyrotropin-releasing hormone affect the synthesis storage and degradation or release of pro lactin will be investigated using primary cultures of rat pituitary cells, amol GH-cells, tumor pitituary cell strains which produce prolactin and growth hormone. Analogs of thyrotropin-releasing hormone which affect synthesis preferentially over release are being synthesized and the ability of these compounds to antagonize TRH-induced prolactin release and to differentiate between prolactin and TSH release will be tested. Estrogen decreases the response of pituitary cells to ergot alkaloids; the mechanism by which this occurs is being investigated.